Sherlock J, Ledwith J, Letteri J
Am J Nephrol. 1984;4(3):158-68. doi: 10.1159/000166797.
A decrease in arterial oxygen tension during hemodialysis has been attributed to a number of factors. In order to more completely define these factors, we studied respiratory gas exchange, arterial blood gases and pH, and dialyzer flux of CO2 during pure ultrafiltration, three types of acetate dialysis, and sorbent regenerated bicarbonate dialysis in which the dialysate concentration of bicarbonate varies. Changes due to position and extracorporeal circulation of a 300-ml volume of blood (sham dialysis) were studied for any effect contributing to the hypoxemia noted with circulation through the membrane and variation in dialysate. Alveolar oxygen tension (PAO2) is calculated by the equation PAO2 = PIO2-PaCO2 (FIO2 + 1-FIO2/RE). RE is the ratio of CO2 excretion by the lung (VCO2) to oxygen consumption (VO2). RE equals RQ (metabolic quotient) when no extrapulmonary CO2 losses occur. Normals in a lounge chair had no change in RE and PAO2. RE decreased to 0.75 during sham dialysis and PAO2 decreased. During pure ultrafiltration RE decreased due to a decrease in VO2 and VCO2 with proportionately greater decrease in VCO2. PAO2 decreased accordingly. Acetate dialysis produced an increase in oxygen consumption without a proportional increase in CO2 excretion and both RQ and RE decreased. When PAO2 decreased during any of these procedures, arterial oxygen tension (PaO2) decreased without a change in A-aO2 gradient. No changes in PaCO2 were noted. RQ did not change during bicarbonate dialysis. At high bicarbonate dialysate concentrations, however, PaCO2 increased and PAO2 decreased. The major reason for hypoxemia during acetate dialysis is a decrease in alveolar oxygen tension due to changes in metabolism and a decrease in pulmonary CO2 excretion when CO2 is lost from the dialyzer. The increasing pH may contribute to the metabolic change during acetate dialysis and the hypoventilation during bicarbonate dialysis. There is little evidence to support an effect of pulmonary capillary obstruction or changes in oxyhemoglobin association on the decrease in arterial oxygen tension observed.
血液透析期间动脉血氧张力降低归因于多种因素。为了更全面地确定这些因素，我们研究了纯超滤、三种醋酸盐透析以及碳酸氢盐透析（其中透析液中碳酸氢盐浓度不同）过程中的呼吸气体交换、动脉血气和pH值以及二氧化碳透析器通量。研究了300毫升血液的体外循环（假透析）因体位变化而产生的影响，以确定其对通过膜循环和透析液变化所导致的低氧血症的作用。肺泡氧张力（PAO2）通过公式PAO2 = PIO2 - PaCO2（FIO2 + 1 - FIO2/RE）计算得出。RE是肺二氧化碳排出量（VCO2）与氧消耗量（VO2）的比值。当无肺外二氧化碳丢失时，RE等于呼吸商（RQ）。在躺椅上的正常人RE和PAO2无变化。假透析期间RE降至0.75，PAO2降低。纯超滤期间，由于VO2和VCO2降低，且VCO2降低幅度更大，RE降低。PAO2相应降低。醋酸盐透析使氧消耗量增加，但二氧化碳排出量未相应增加，RQ和RE均降低。在这些操作过程中，当PAO2降低时，动脉血氧张力（PaO2）降低，而肺泡 - 动脉血氧分压差（A - aO2）梯度无变化。未观察到PaCO2有变化。碳酸氢盐透析期间RQ无变化。然而，在高碳酸氢盐透析液浓度时，PaCO2升高，PAO2降低。醋酸盐透析期间低氧血症的主要原因是代谢变化导致肺泡氧张力降低以及透析器二氧化碳丢失时肺二氧化碳排出减少。pH值升高可能导致醋酸盐透析期间的代谢变化以及碳酸氢盐透析期间的通气不足。几乎没有证据支持肺毛细血管阻塞或氧合血红蛋白结合变化对观察到的动脉血氧张力降低有影响。
